Transcriptional activation of c‐fos by oncogenic Ha‐Ras in mouse mammary epithelial cells requires the combined activities of PKC‐λ, ϵ and ζ
Transcriptional activation of c‐fos by oncogenic Ha‐Ras in mouse mammary epithelial cells requires the combined activities of PKC‐λ, ϵ and ζ
复制标题
小鼠乳腺上皮细胞中致癌 Ha-Ras 对 c-fos 的转录激活需要 PKC-λ、ϵ 和 ζ 的联合活性
DOI：
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
F. Überall
中科院分区：
文献类型：
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作者：
S. Kampfer;K. Hellbert;A. Villunger;W. Doppler;G. Baier;H. Grunicke;F. Überall
蛋白激酶C （PKC）异构体cPKC‐α、nPKC‐柱、aPKC‐λ和aPKC‐ζ通过转化Ha‐Ras在C‐fos启动子驱动的CAT‐报告结构的转录激活中的意义已经被研究。这是通过使用反义结构体编码RNA，直接针对相应mRNA的亚型特异性5 '序列，以及PKC突变体的表达来实现的，这些突变体代表PKC亚型的激酶缺陷、显性阴性或组成活性形式。数据表明，在HC11小鼠乳腺上皮细胞中，转化Ha‐Ras需要三种PKC同工酶的活性：aPKC‐λ， nPKC‐λ和aPKC‐ζ，而不是cPKC‐α，来激活c‐fos的转录。致癌Ha - Ras与各种PKC同工酶的激酶缺陷、显性阴性和组成活性突变体组合的Co -表达与一个初步模型一致，该模型表明，在从Ha - Ras到c - fos启动子的信号通路中，aPKC‐λ作用于上游，而aPKC‐ζ作用于nPKC‐ε的下游。
The implication of protein kinase C (PKC) isoforms cPKC‐α, nPKC‐ϵ, aPKC‐λ and aPKC‐ζ in the transcriptional activation of a c‐fos promoter‐driven CAT‐reporter construct by transforming Ha‐Ras has been investigated. This was achieved by employing antisense constructs encoding RNA directed against isoform‐specific 5′ sequences of the corresponding mRNA, and expression of PKC mutants representing either kinase‐defective, dominant negative, or constitutively active forms of the PKC isoforms. The data indicate that in HC11 mouse mammary epithelial cells, transforming Ha‐Ras requires the activities of the three PKC isozymes: aPKC‐λ, nPKC‐ϵ and aPKC‐ζ, not, however, of cPKC‐α, for the transcriptional activation of c‐fos. Co‐expression of oncogenic Ha‐Ras with combinations of kinase‐defective, dominant negative and constitutively active mutants of the various PKC isozymes are in agreement with a tentative model suggesting that, in the signaling pathway from Ha‐Ras to the c‐fos promoter, aPKC‐λ acts upstream whereas aPKC‐ζ functions downstream of nPKC‐ϵ.
影响因子：
11.2
作者：
C. T. Powell;J. Gschwend;W. Fair;N. Brittis;D. Stec;R. Huryk
通讯作者：
C. T. Powell;J. Gschwend;W. Fair;N. Brittis;D. Stec;R. Huryk
DOI：
10.1016/s0021-9258(18)82231-1
发表时间：
1993-05
期刊：
The Journal of biological chemistry
影响因子：
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作者：
K. Ha;J. Exton
通讯作者：
K. Ha;J. Exton
蛋白激酶 C beta 1 和蛋白激酶 C beta 2 激活 p57 丝裂原激活蛋白激酶并阻断结肠癌细胞的分化。
DOI：
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发表时间：
1996
期刊：
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
影响因子：
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作者：
Sauma,S;Yan,Z;Ohno,S;Friedman,E
通讯作者：
Friedman,E